| First Author | Nakaya T | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 9 | Pages | 5180-7 |
| PubMed ID | 20870947 | Mgi Jnum | J:166080 |
| Mgi Id | MGI:4839685 | Doi | 10.4049/jimmunol.1002026 |
| Citation | Nakaya T, et al. (2010) Critical role of Pcid2 in B cell survival through the regulation of MAD2 expression. J Immunol 185(9):5180-7 |
| abstractText | The mitotic checkpoint is essential for maintaining genomic stability in differentiating B cells undergoing genetic alterations of the Ig gene. In this study, using real-time RT-PCR and in situ RNA hybridization, we demonstrated that MAD2 mRNA export is selectively regulated by Pcid2/Thp1. Pcid2 small interfering RNA induced a cell-cycle abnormality with increased apoptosis and polyploidy, as previously observed in MAD2-knockdown cells. Pcid2 small interfering RNA reduced MAD2 expression, but not the expression of other cell-cycle checkpoint proteins, such as MAD1 and BUBR1, or the cell-cycle-associated proteins, cyclin A, cyclin B1, and cyclin-dependent kinase 1. In mouse B lineage cells, Pcid2 transcripts appeared in a stage-dependent manner at high levels in bone marrow pre-B and immature B cells, and in spleen transitional 1 and follicular B cells, but at lower levels in pro-B, transitional 2, and marginal zone B cells, suggesting a stage-dependent requirement for MAD2 regulation. Cd19-cre-derived targeting of the Pcid2 gene induced a mature B cell deficiency in mice. These findings indicate that Pcid2 is essential for B cell survival through the regulation of MAD2 expression during B cell differentiation. |
